Light/dye microvascular injury eliminates pial arteriolar dilation in hypotensive piglets.

Cerebral vasodilation in response to hypotension is necessary to maintain adequate cerebral blood flow. This study in newborn pigs examines the hypothesis that endothelial injury in vivo inhibits cerebral vasodilation in response to hypotension in newborn pigs, thus suggesting that this response is endothelium dependent. Chloralose-anesthetized piglets with closed cranial windows were studied before and after injury caused by light/dye or before and after dye only sham control. Light/dye injury was produced by injecting sodium fluorescein i.v. and passing filtered light from a mercury arc lamp through the cranial window. Measurements of pial arteries and arterioles were made during normotensive and hypotensive periods. Hemorrhagic hypotension (to 50% of the mean arterial control value) caused pial arterial and arteriolar diameters to increase 49 +/- 8% and 66 +/- 8%, respectively. After the light/dye injury, dilation in response to hypotension was absent, whereas dilations in response to isoproterenol and constriction in response to hypertension (3.33 to 4.0 kPa increase in arterial pressure) and hypocapnia were retained. These findings are consistent with the hypothesis that hypotension-induced cerebral arteriolar vasodilation is dependent on endothelial signals influencing adjacent smooth muscle.